title: Exaggerated increase of exercise-induced pulmonary artery pressure in systemic sclerosis patients predominantly results from left ventricular diastolic dysfunction.
abstract: OBJECTIVE
  High prevalence of exaggerated pulmonary artery pressure response to exercise (EPAPR) was reported in patients with systemic sclerosis (SSc). However, pathophysiology of this phenomenon has not been well defined. Therefore, we evaluated the frequency and potential aetiology of EPAPR in SSc patients.
  
  
  METHODS
  We included 85 patients (79 female, 6 male, mean age 54.3 ± 13.9 years) with SSc. Transthoracic echocardiography followed by exercise Doppler echocardiography (EDE) were performed. A positive EDE was defined when at least 20 mmHg increase of tricuspid regurgitation peak gradient (TRPG) was recorded. Right heart catheterization (RHC) with exercise was performed in positive EDE patients and in subjects with resting TRPG >31 mmHg.
  
  
  RESULTS
  Resting TRPG >31 mmHg and/or positive EDE was found in 30 patients and they were referred to RHC. Finally, RHC was performed in 20 patients (16 pts resting TRPG >31 mmHg and 4 others normal resting TRPG and positive EDE). In 12 (60 %) of them an EPAPR with elevated pulmonary capillary wedge pressure (PCWP) was observed. Interestingly, mean left atrium (LA) diameter was greater in an EPAPR with elevated PCWP patients than in subjects with normal exercise response (39.36 ± 5.6 vs. 35.53 ± 3.48, p = 0.03). In EPAPR with elevated PCWP group greater mean value of E/E' of mitral lateral annulus was observed (7.98 ± 3.35 vs. 6.27 ± 1.94, p = 0.03). In the univariate logistic regression analysis increased LA diameter was significant predictor of EPAPR with elevated PCWP (OR 1.199, 95 % CI 1.029-1.396, p = 0.019).
  
  
  CONCLUSIONS
  Despite very well-known risk of PAH in systemic sclerosis patients, the excessive increase of PAP during exercise is more commonly caused by left ventricular diastolic dysfunction than pulmonary arterial vasculopathy.
authors.affiliation: Department of Internal Medicine and Cardiology, Medical University of Warsaw, Warsaw, Poland, michal.ciurzynski@wum.edu.pl.
authors.forename: Michał
authors.initials: M
authors.lastname: Ciurzyński
authors.forename: Piotr
authors.initials: P
authors.lastname: Bienias
authors.forename: Katarzyna
authors.initials: K
authors.lastname: Irzyk
authors.forename: Maciej
authors.initials: M
authors.lastname: Kostrubiec
authors.forename: Zbigniew
authors.initials: Z
authors.lastname: Bartoszewicz
authors.forename: Maria
authors.initials: M
authors.lastname: Siwicka
authors.forename: Marcin
authors.initials: M
authors.lastname: Kurzyna
authors.forename: Urszula
authors.initials: U
authors.lastname: Demkow
authors.forename: Piotr
authors.initials: P
authors.lastname: Pruszczyk
mesh_terms: D000328:Adult; D000368:Aged; D062186:Arterial Pressure; D006328:Cardiac Catheterization / Q000379:methods*; D004452:Echocardiography; D015150:Echocardiography, Doppler; D015444:Exercise / Q000502:physiology; D005080:Exercise Test; D005260:Female; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D011651:Pulmonary Artery; D011669:Pulmonary Wedge Pressure; D012595:Scleroderma, Systemic / Q000503:physiopathology*; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology*